Ca2+ and acidosis synergistically lead to the dysfunction of cortical GABAergic neurons during ischemia

Biochemical and Biophysical Research Communications

Volumn 394, Issue 3, 2010, Pages 709-714

  Huang, Li ^a,b   Chen, Na ^a   Ge, Ming ^b   Zhu, Yan ^b   Guan, Sudong ^b   Wang, Jin Hui ^a,b  

^a BENGBU MEDICAL COLLEGE   (China)

^b INSTITUTE OF BIOPHYSICS   (China)

Author keywords

Acidosis; Action potential; Calcium; Cortex; GABAergic neuron; Ischemia

Indexed keywords

4 AMINOBUTYRIC ACID RECEPTOR; CALCIUM ION; PROTON; SODIUM CHANNEL; 4 AMINOBUTYRIC ACID; CALCIUM;

ACIDOSIS; ACTION POTENTIAL; ANIMAL CELL; ANIMAL TISSUE; ARTICLE; BRAIN ISCHEMIA; BRAIN SLICE; CONTROLLED STUDY; EXCITOTOXICITY; MEMBRANE POTENTIAL; MOUSE; NONHUMAN; PATCH CLAMP; PRIORITY JOURNAL; ANIMAL; APOPTOSIS; METABOLISM; MOUSE STRAIN; NERVE CELL; PATHOLOGY; PATHOPHYSIOLOGY;

ACIDOSIS; ANIMALS; APOPTOSIS; BRAIN ISCHEMIA; CALCIUM; GAMMA-AMINOBUTYRIC ACID; MICE; MICE, INBRED STRAINS; NEURONS;

EID: 77950519469     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2010.03.056     Document Type: Article

References (27)

1. Broughton B.R., Reutens D.C., and Sobey C.G. Apoptotic mechanisms after cerebral ischemia. Stroke 40 5 (2009) e331-e339
2. Hou S.T., and MacManus J.P. Molecular mechanisms of cerebral ischemia-induced neuronal death. Int. Rev. Cytol. 221 (2002) 93-148
3. Choi D.W. Calcium-mediated neurotoxicity: relationship to specific channel types and role in ischemic damage. Trends Neurosci. 11 10 (1988) 465-469
4. Won S.J., Kim D.Y., and Gwag B.J. Cellular and molecular pathways of ischemic neuronal death. J. Biochem. Mol. Biol. 35 1 (2002) 67-86
5. Camacho A., and Massieu L. Role of glutamate transporters in the clearance and release of glutamate during ischemia and its relation to neuronal death. Arch. Med. Res. 37 1 (2006) 11-18
6. Inage Y.W., Itoh M., Wada K., and Takashima S. Expression of two glutamate transporters, GLAST and EAAT4, in the human cerebellum: their correlation in development and neonatal hypoxia-ischemic damage. J. Neuropathol. Exp. Neurol. 57 6 (1998) 554-562
7. Yamashita A., Makita K., Kuroiwa T., and Tanaka K. Glutamate transporters GLAST and EAAT4 regulate postischemic Purkinje cell death: an in vivo study using a cardiac arrest model in mice lacking GLAST or EAAT4. Neurosci. Res. 55 3 (2006) 264-270
8. Block F. Global ischemia and behavioral deficits. Prog. Neurobiol. 58 (1999) 279-295
9. Lipton P. Ischemic cell death in brain neurons. Physiol. Rev. 79 4 (1999) 1431-1568
10. Metha S.L., Manhas N., and Raghubir R. Molecular targets in cerebral ischemia for developing novel therapeutics. Brain Res. Rev. 54 1 (2007) 34-66
11. Schwartz-Bloom R.D., and Sah R. R-aminobutyric acid A neurotransmission and cerebral ischemia. J. Neurochem. 77 (2001) 353-371
12. White B.C., Sullivan J.M., DeGracia D.J., O'Neil B.J., Neumar R.W., Grossman L.I., Rafols J.A., and Krause G.S. Brain ischemia and reperfusion: molecular mechanisms of neuronal injury. J. Neurol. Sci. 179 (2000) 1-33
13. Welsh J.P., Yuen G., Placantonkis D.G., Yu T.Q., Haiss F., O'Heaen E., Molliver M.E., and Aicher S.A. Why do Purkinje cells die so easily after global brain ischemia? Aldolase C, EAAT4, and the cerebellar contribution to posthypoxic myoclonus. Adv. Neurol. 89 (2002) 331-359
14. Dalkara T., and Moskowitz M.A. Recent developments in the experimental stroke. NeuroSci. News 2 (1999) 20-27
15. Devasenapathy A., and Hachinski V.C. Current treatment of acute ischemic stroke. NeuroSci. News 2 (1999) 4-13
16. Taoufik E., and Probert L. Ischemic neuronal damage. Curr. Pharm. Des. 14 33 (2008) 3565-3573
17. Wang J.-H. Short-term cerebral ischemia causes the dysfunction of interneurons and more excitation of pyramidal neurons. Brain Res. Bull. 60 1-2 (2003) 53-58
18. 2+ elevation in cerebellar slices: a comparative study with the values found in hippocampal slices. Acta Neuropathol. (Berl.) 89 1 (1995) 2-7
19. 2+. Biochem. Biophys. Res. Commun. 366 (2008) 401-407
20. Simon R., and Xiong Z. Acidotoxicity in brain ischemia. Biochem. Soc. Trans. 34 (2006) 1356-1361
21. Chen N., Chen X., and Wang J.-H. Homeostasis established by coordination of subcellular compartment plasticity improves spike encoding. J. Cell Sci. 121 17 (2008) 2961-2971
22. 2+, and acidosis-mediated neuronal injury by intracellular injury. J. Biol. Chem. 281 39 (2006) 29369-29378
23. Chen N., Chen S.L., Wu Y.L., and Wang J.H. The refractory periods and threshold potentials of sequential spikes measured by whole-cell recordings. Biochem. Biophys. Res. Commun. 340 (2006) 151-157
24. 2+/CaM induces synaptic potentiation requiring CaM-KII and PKC activity. Neuron 15 2 (1995) 443-452
25. Chen N., Zhu Y., Gao X., Guan S., and Wang J.-H. Sodium channel-mediated intrinsic mechanisms underlying the differences of spike programming among GABAergic neurons. Biochem. Biophys. Res. Commun. 346 (2006) 281-287
26. Donnan G.A., and Davis S.M. Neuroprotection: still achievable in humans. Stroke 39 2 (2008) 525
27. Hussain M.S., and Shuaib A. Research into neuroprotection must continue. But with a different approach. Stroke 39 2 (2008) 1-2